Evidence map›Paper›PMID 22963644›Full record

ReviewJournal of child psychology and psychiatry, and allied disciplines2013

What have we learnt about the causes of ADHD?

Anita Thapar, Miriam Cooper, Olga Eyre, Kate Langley

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of child psychology and psychiatry, and allied disciplines, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers, 15 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
271citing papers in PubMed, 15 pooled it
23.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

271 citing papers in PubMed, 15 syntheses or guidelines pooled it, 694 citations in OpenAlex.

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  9. Parental Age and the Risk of ADHD in Offspring: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2021
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  11. Pathogens and global health · 2020
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211 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Anita ThaparChild & Adolescent Psychiatry Section, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Cardiff, UK. thapar@cf.ac.uk
Miriam Cooper
Olga Eyre
Kate Langley
Cardiff University · GB

Funding

Medical Research Council G1000632Medical Research Council G9810900Wellcome Trust
6 · The paper itself

Abstract

backgroundAttention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been considered as potential risk factors.

methodThis review (focussing on literature published since 1997, selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and selected environmental risks, examines their relationships with ADHD and discusses the likelihood that these risks are causal as well as some of the main implications.

resultsNo single risk factor explains ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders. Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal. There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that go beyond simply testing for association are beginning to contest the robustness of some environmental exposures previously thought to be ADHD risk factors.

conclusionsThe genetic risks implicated in ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond what is predicted by a family history. There is a need to consider the possibility of parents and siblings being similarly affected and how this might impact on engagement with families, influence interventions and require integration with adult services. Genetic contributions to disorder do not necessarily mean that medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic and aetiological research findings and impart informed explanations to families.

Indexed as

EnvironmentGene-Environment InteractionGenetic Predisposition to DiseaseAttention Deficit Disorder with HyperactivityComorbidityDevelopmental DisabilitiesFemaleHumansPregnancyPrenatal Exposure Delayed EffectsPsychosocial DeprivationRisk Factors

Identifiers

PMID22963644
PMCPMC3572580
OpenAlexW1791898768

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.